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非靶向血清代谢组学揭示了白金平喘通过初级胆汁酸生物合成减轻卵清蛋白诱导的哮喘。

Untargeted serum metabonomic reveals alleviated ovalbumin-induced asthma by Baijin Pingchuan through primary bile acid biosynthesis.

作者信息

Lizhong Ding, Qiang Zhang, Yingying Sun, Yibu Kong, Yongfu Song, Yongji Wang

机构信息

Department of Pediatrics, the Affiliated hospital to Changchun University of Chinese Medicine, Changchun 130017, China.

出版信息

J Tradit Chin Med. 2024 Dec;44(6):1187-1193. doi: 10.19852/j.cnki.jtcm.2024.06.007.

Abstract

OBJECTIVE

To investigate the effect of baijinpingchuan (, BJPC) on the asthma rat model and identify differential metabolites and disturbed metabolic pathways.

METHODS

The rats were categorized into six groups: control, dexamethasone (DEX), ovalbumin (OVA), and low-, median-, and high-dose BJPC. The rats, except for the control group, were initially treated with OVA to develop the asthma model, which was then activated using DEX, OVA, and low-, median-, and high-dose BJPC. Enzyme-linked immunosorbent assay kit was used to detect the expression of interleukin (IL)-33, IL-25, thymic stromal lymphopoietin (TSLP), and transforming growth factor-beta 1 (TGF-β1). Hematoxylin and eosin staining were performed to observe the pathological condition of the lung. Untargeted serum metabonomic analysis was conducted to identify differential metabolites and disturbed metabolic pathways.

RESULTS

High-dose BJPC significantly inhibited the expression of IL-33, IL-25, TSLP, and TGF-β1 ( 0.0001). Further, high-dose BJPC improved inflammatory cell infiltration, which plays a similar role in asthma as DEX. OVA-induced and BJPC-treated rats were identified through 17 differential metabolites, especially cholic acid. Furthermore, primary bile acid biosynthesis was a significantly differential pathway in the mechanism of BJPC for treating asthma.

CONCLUSIONS

BJPC plays an anti-inflammation role in asthma, which might be a promising therapy through mediating primary bile acid biosynthesis.

摘要

目的

探讨白荆平喘(BJPC)对哮喘大鼠模型的影响,并鉴定差异代谢物和受干扰的代谢途径。

方法

将大鼠分为六组:对照组、地塞米松(DEX)组、卵清蛋白(OVA)组以及低、中、高剂量BJPC组。除对照组外,其余大鼠先用OVA诱导建立哮喘模型,然后分别用DEX、OVA以及低、中、高剂量BJPC进行处理。采用酶联免疫吸附测定试剂盒检测白细胞介素(IL)-33、IL-25、胸腺基质淋巴细胞生成素(TSLP)和转化生长因子-β1(TGF-β1)的表达。进行苏木精-伊红染色以观察肺组织的病理状况。进行非靶向血清代谢组学分析以鉴定差异代谢物和受干扰的代谢途径。

结果

高剂量BJPC显著抑制IL-33、IL-25、TSLP和TGF-β1的表达(<0.0001)。此外,高剂量BJPC改善了炎症细胞浸润,其在哮喘中的作用与DEX相似。通过17种差异代谢物鉴定出OVA诱导并经BJPC处理的大鼠,尤其是胆酸。此外,初级胆汁酸生物合成是BJPC治疗哮喘机制中的一条显著差异途径。

结论

BJPC在哮喘中发挥抗炎作用,可能是一种通过介导初级胆汁酸生物合成的有前景的治疗方法。

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